Acute leukemia ranks as the malignancy of highest incidence in the pediatric population of the United States. Despite the recent epidemiologic data which suggests that environmental carcinogens may be responsible for most of human cancer, chemical carcinogens are seldom considered as etiologic agents in pediatric neoplasms. The proposed research will examine the ontogenetic expression of aryl hydrocarbon hydroxylase, glutathione-S-transferase and epoxide hydrase in human lymphocytes and elucidate the patterns of expression of these enzyme activities in children with acute leukemia. This work should permit the recognition of developmental factors which affect the susceptibility of infants and children to the neoplastic effects of chemical carcinogens. It will also provide important insight with respect to the ability of the human fetus to interact with its chemical environment. Finally, the patterns of expression of these enzyme activities in acute leukemia will provide a basis for assessing the relative importance of ontogeny and genetics in the proposed association between chemical carcinogens and pediatric malignancy.